Cardiovascular management Flashcards

1
Q

What are the risk factors of CVD

A
  • Smoking
  • Family history
  • Diabetes
  • Hypertension
  • Ethnic background
  • Physical inactivity
  • Sex
  • Age
  • BMI over 25
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2
Q

What lifestyle changes could help decrease CVD risk?

A
  • Cardioprotective diet
  • Physical activity
  • Smoking cessation
  • Weight management
  • Alcohol consumption reduction
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3
Q

What is the first pharmacological intervention for CVD?

A

Lipid modification therapy
- Statins –> Primary prevention: Atorvastatin 20mg/day

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4
Q

What do statins do?

A

Inhibit cholesterol and LDL production by inhibiting the enzyme HMG-CoA reductase –> which plays a central role in cholesterol production in the liver

Also has some effect of increasing HDL

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5
Q

Who are offered Atorvastatins?

A
  • CVD primary prevention (10% risk of CVD in 10 years)
  • High CVD risk
  • Previous CVD
  • Type 1 and 2 diabetes
  • Patients with CKD
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6
Q

What are some side effects of statins?

A

Muscle pain and weakness, nose bleeds, sore throat, headache, hyperglycaemia, increased diabetes risk

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7
Q

What statins does grapefruit juice interfere with and how?

A

Atorvastatin and Simvastatin

It increases the absorption in blood and increases chance of side effects

A small glass can be had occasionally when taking Atorvastatin, it only has effect when in large quantities

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8
Q

What is Inclinsiran?
How is it taken?

A

A cholesterol lowering drug for people with primary hypercholesterolemia or mixed dyslipidemia who already have had a cardiovascular event.

Twice yearly injections

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9
Q

How does Inclinsiran work?

A

It uses RNA interference to boost the liver’s ability to remove harmful cholesterol from the body.

Mechanism:
- Propotein convertase subtilisin-kexin type 9 (PCSK9) binds to LDL receptors and targets receptors for lysosomal degradation
- Small interfering RNA (siRNA) molecules target the hepatic production of PCSK9.
- Inclinsirin is a long-acting synthetic siRNA directed against PCSK9 to significantly reduce hepatic production of PCSK9 causing reduction in LDL cholesterol levels.

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10
Q

What is hypertension?

A

High blood pressure
Narrowing of the blood vessel wall, vasoconstriction, and increased blood flow can all cause high blood pressure.

Leading risk factor for CHD in UK
50% of strokes and heart attacks is associated with high blood pressure

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11
Q

What maintains healthy blood pressure

A
  • Baroreceptors
  • Peripheral chemoreceptors
  • Vascular endothelium
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12
Q

Describe primary hypertension

A

Caused by obesity, smoking, stress
Accounts for 90% of hypertension cases
Leads to increased sympathetic nervous system activity (increased cardiac output)

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13
Q

Describe secondary hypertension

A

Caused by heart disease, renal disease, adrenal tumour, effect of medications
Accounts for less that 10% of hypertension cases

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14
Q

What are some complications of hypertension?

A
  • TIA
  • Renal failure
  • Peripheral vascular disease
  • Heart failure
  • Coronary heart disease
  • Left ventricular hypertrophy
  • Retinopathy
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15
Q

How does hypertension causes damage?

A

Smooth muscle cells in the arterial wall multiply and enlarge
Walls become thicker and the opening becomes smaller causing the pressure in the lumen to increase.

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16
Q

What are the different stages of hypertension and the BP associated with them?

A

Normal - 120/80mmHg
Prehypertension - 135/85mmHg
Stage one hypertension - 135/85 - 149/94mmHg
Stage two hypertension - >150/95mmHg

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17
Q

What are some examples of ACE inhibitors?

A

Lisinopril, Ramipril, Enalapril

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18
Q

How do ACE inhibitors work?

A
  • Blocks production of Angiotensin II
  • Leads to vasodilation and diuresis
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19
Q

Describe the process of increased blood pressure in the body.
Include processes at liver, lungs, kidney and adrenal cortex.

A
  1. Liver produces Angiotensinogen
  2. Renin (produced by the kidney) converts Angiotensinogen into Angiotensin I
  3. A the lungs, Angiotensin-converting enzyme converts type 1 into type 2
  4. Angiotensin II stimulates the adrenal glands to secrete aldosterone
  5. Aldosterone causes the kidneys to reabsorb sodium and water from urine and secrete potassium
  6. Low blood volume causes the kidney to secrete renin (used in step 1)
  7. Sodium and water retention from the kidney leads to increased blood pressure
  8. Angiotensin II causes blood vessels to constrict
  9. Vasocontriction
  10. Increased blood pressure
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20
Q

What is aldosterone?

A

A protein which causes the blood vessels to constrict and counteract low blood pressure

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21
Q

What are some examples of Angiotensin II receptor blockers?

A

Candesartan, Azilsartin, Losartan

22
Q

What do Angiotensin II receptor blockers do?

A

Block effects of Angiotensin II
Blood vessels are allowed to dilate and blood pressure is reduced

23
Q

Give some examples of calcium channel blockers

A

Amlodipine, Nifedipine, Verapamil

24
Q

What do calcium channel blockers do?

A

Blocks effects of calcium on blood vessels
Calcium taken up by blood vessel walls to cause contraction
CCBs allow blood vessel walls to relax and dilate

25
Q

What are some side effects of CCBs?

A

Abdominal pain, nausea, vomiting, dizziness, drowsiness, erectile dysfunction, flushing, gingival hyperplasia, myalgia, palpitations and tachycardia, peripheral oedema, skin reactions

26
Q

What can CCBs interact with?

A

Alpha blockers
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Diuretics
Antipsychotics
- Cause enhanced antihypertensive effect

Beta blockers
- Hypotensive effect enhanced, extreme caution needed for Verepamil or Diltiazem due to the risk of significant adverse cardiac events

Statins
- Some interaction, dose adjustment may be needed

NSAIDs
- Hypotensive effect of CCB may be reduced with concurrent use

Grapefruit
- Increase exposure to CCB

St John’s Wort
- Plasma concentrations of CCB may be reduced

27
Q

What can ARBs interact with?

A

Angiotensin-converting enzyme inhibitors
- Increase risk of hyperkalemia, hypotension and renal impairment
- Those with diabetic neuropathy are particularly susceptible to hyperkalemia and should not receive combination treatment

Diuretics
- May cause volume depletion and a risk of hypotension

Lithium
- Increases in the serum lithium concentrations and toxicity

NSAIDs
- Renal risks, attenuation of the antihypertensive effect

Alpha blockers, antiphysychotics, beta blockers, CCBs, tricyclic antidepressants
- Enhanced hypotensive effect

28
Q

Who should avoid Thiazide-like diuretics?

A

People with
- Hyponatraemia
- Hypercalcaemia
- Refractory hypokalaemia
- Addison’s disease
- Severe liver disease
- Severe renal impairment
Pregnant women

29
Q

What are some side effects of Thiazide-like diuretics?

A

Postural hypotension, hyperglycaemia, hypokalaemia, electrolyte imbalances, cardiac arrhythmias, dizziness, headaches, ED, blood and lymphatic system disorders

Elderly may be more susceptible to adverse effects

30
Q

What can interact with Thiazide-like diuretics?

A

ACE inhibitors and ARBs
- Can cause rapid fall in blood pressure in a person who is volume depleted

Alpha-blockers
- Enhanced hypotensive effect and increased risk of first-dose hypotension

NSAIDs and Cox-2 inhibitors
- Increased risk of nephrotoxicity and antagonism of diuretic effect with concomitant use

Corticosteroids
- May potentiate the hypokalemia

Insulin and oral anti-diabetes agents
- May require dose adjustment

Calcium salts
- May increase the risk of hypercalcemia when given concurrently

Tricyclic antidepressants
- Increased risk of postural hypotension

CCBs, Beta-blockers, hypnotics, nitrates
- Enhanced hypotensive effect

31
Q

What are some side effects of ACE inhibitors?

A

Renal impairment, hyperkalaemia, cough, angio-edema, dizziness and headaches, hepato-biliary disorders, abdominal discomfort, alopecia, chest pain or angina, constipation, diarrhoea, drowsiness, muscle spasms, nausea and vomiting

32
Q

What can interact with ACE inhibitors?

A

ARBs and Aliskerin
- Effects on the renin-angiotensin system increase the risk of hyperkalemia, hypotension, and renal impairment
- Not suitable for those with diabetic neuropathy

Diuretics
- Cause rapid fall in blood volume in a person who is volume depleted

Bee/ wasp venom extracts
- Risk of severe anaphylaxis

NSAIDs
- Increased risk of renal impairment and hypotensive effect antagonised

Antacids
- Possible decreased absorption of ACE inhibitor

Alpha-blockers, antipsychotics, beta-blockers, CCBS, hypnotics, SGLT2 inhibitors, nitrates
- Enhanced hypotensive effect

Insulin and oral antidiabetic agents
- Enhanced hypoglycaemia effect

Heparin
- Risk of hyperkalemia

NSAIDs and COX-2 inhibitions
- Attuenute the antihypertensive effect and increase the risk of deteriorating renal function and hyperkalemia

33
Q

What can interact with Beta-blockers?

A

Alpha-blockers, ACE inhibitors, ARBs, diuretics, nitrates,
- Enhanced hypotensive effect

Antidepressants
- Increased risk of postural hypotension

CCBs
- Risk of bradycardia, asystole, severe hypotension and heart failure

Insulin and anti-diabetic agents
- Risk of exacerbation of blood sugar lowering effects and symptoms of hypoglycaemia may be masked

NSAIDs
- Hypotensive effect antagonised with concomitant use

34
Q

What are some side effects from Alpha-blockers?

A

Chest pain, constipation, and diarrhoea, depression, drowsiness, first dose hypotension, headache, nausea, palpitation, postural hypotension, skin reactions, weakness

35
Q

What can interact with Alpha-blockers?

A

ACE inhibitors, ARBs, antipsychotics, beta-blockers, CCBs, diuretics, hypnotics, moxonidine, nitrates
- Enhanced hypotensive effect

Moxisylyte
- Increased risk of severe postural hypotension

36
Q

Where does each type of diuretic have effect?

A

Loop - Loop of Henle to the medulla
Thiazide - Proximal part of the distal tubule
K+ sparing - Distal tubule to the collecting duct

37
Q

How do diuretics help with hypertension?

A

They increase sodium and water excretion from the kidney, causing plasma volume to fall

38
Q

How do loop diuretics work?
Give an example of one

A

The inhibit Na, Cl and K reabsorption from the loop to the medulla reducing concentration within the medulla and osmotic pressure causing less H2O to be reabsorbed

Frusemide

39
Q

How do Thiazide diuretics work?
Give an example of one

A

Act on the nephron mainly at the proximal part of the distal tubule
Risk of hypokalemia due to urinary potassium loss

Bendroflumethiazide

40
Q

How do Beta-blockers help with hypotension?

A

They bind to beta-adrenoreceptors which block the binding of norepinephrine and epinephrine to these receptors.
Causes a reduction in heart rate
Reduces renin release from the kidneys which in turn reduces the conversion of Angiotensinogen to Angiotensin I which reduces the pathway to cause vasoconstriction and overall increased blood pressure

41
Q

What are some examples of Beta-blockers?

A

Propanol, Atenolol, Pindol

42
Q

How do Alpha-blockers help with hypotension?

A

Antagonist of alpha-adrenergic receptors
Prevent the stimulation of adrenergic receptors responsible for increased blood pressure
- Reduce to tone in blood vessels
- Vasodilation –> Peripheral resistance reduced

43
Q

Give an outline of Antihypertensive therapy

A

Step one
- Lifestyle changes

  • Monotherapy –> ACE inhibitors, ARBs, CCB

Step two
- Drug combination of two drugs

Step three
- Drug combination of three drugs –> ACEi or ARBs + CCB + Thiazide-like diuretics

Step four
- Seek expert advise and/or add low dose spironolactone if blood potassium is below 4.5mmol/l or adding alpha or beta-blockers if its above 4.5mmol/l

44
Q

What helps with angina management?

A
  • Nitrates
  • Beta-blockers
  • CCBs
  • Aspirin/ Clopidogrel (stop blood clotting)

+

  • Lifestyle changes
  • Surgery
45
Q

What are some signs and symptoms of cardiac failure?

A
  • Increased night urination
  • Shortness of breath
  • Difficulty sleeping due to breathing problems
  • Swelling of feet and legs
  • Chronic fatigue
  • Swollen or tender abdomen with appetite loss
  • Cough with frothy sputum
  • Confusion and/ or impaired memory
46
Q

How do nitrates help with angina management?

A

Increase venous cacipitance
Dilates coronary blood vessels and improves oxygen supply to the heart muscles
Dilates peripheral arteries

Most effective taken as soon as pain occurs

47
Q

What are the treatment options for cardiac failure?

A

First line - ACE inhibitors and Beta-blockers
Additional treatments include ARBs and diuretics

Lifestyle advice
- Restrict fluids for people with dilutional hyponatraemia
- Reduced intake of salt and fluid for those with high levels of salt and or/ fluid consumption
- Avoid salt substitutes that contain potassium

48
Q

What can help reduce CVD risk?
(not primary or secondary prevention)

A
  • Fibrates –> Activate PPAR, increasing lipid metabolism, decreasing LDL
  • Nicotinic acid –> has an effect on liver health
  • Bile acid sequestrants (anion exchange resins) –> bind to bile to reduce absorption
  • Omega-3 fatty acid compounds –> reduce inflammation
  • Plant stanols and sterols –> help reduce cholesterol levels

Ezetimibe can be offered fro primary hypercholesterolemia –> reducing cholesterol absorption in small intestine

49
Q

What is the cardio-protective diet?

A
  • Less saturated fat
  • Choose foods containing mono-unsaturated fats (olive oil and rapeseed oil) and polyunsaturated fat (corn oil and sunflower oil)
  • Reduce sugar intake
  • Choose healthy ways of cooking and preparing food
  • Choose wholegrain varieties of starchy food
  • Eat 5 a day
  • Eat at least two portions of fish a week, including a portion of oily fish
  • Eat at least 4-5 portions of unsalted nuts, seeds and legumes a week
50
Q

What are some causes of cardiac failure?

A

Myocardial infaction causes 70% of cases
- Loss of oxygen and nutrients damages the hearts muscle tissue causing some parts to atrophy
- Remaining tissue has to work even harder

Hypotension 7% of causes

Other causes
- Abnormal heart values
- Heart muscle disease
- Congenital heart disease

51
Q

For step two of Antihypertensive therapy, what drugs can work in combination?

A

ACE inhibitor OR ARBs + CCB OR Thizide-like diuretic

CCB + ACE inhibitor OR Thiazide-like diuretic